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Dexmedetomidine sedation in a pediatric cardiac patient scheduled for MRI

[Sédation avec dexmédétomidine chez une enfant devant subir un examen d’IRM]

From the Department of Anesthesiology, Ochsner Clinic Foundation, New Orleans, Louisiana, USA.

Address correspondence to: Dr. Elizabeth T. Young, Ochsner Clinic Foundation, 1514 Jefferson Highway, New Orleans, LA 70121, USA. Phone 504-842-3755; Fax 504-842-2036; E-mail: Eyoung{at}ochsner.org

	Abstract

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Purpose: To describe the use of dexmedetomidine for sedation in a critically ill infant undergoing magnetic resonance imaging (MRI).

Clinical features: A nine-month-old 5.1 kg infant was to have an MRI study of the thorax. The infant had multiple congenital cardiac anomalies which had been partially corrected surgically. After administration of atropine, 0.1 mg iv, a loading dose of dexmedetomidine (1 µg·kg^–1 iv) was administered over ten minutes followed by a continuous infusion of 0.5 µg·kg^–1·hr^–1 for maintenance. Propofol 5 mg iv were administered after the loading dose of dexemedetomidine to produce somnolence. Anesthetic conditions for performing the MRI were excellent. The infant remained motionless, breathing spontaneously. Hemodynamics remained stable throughout the procedure. Recovery was rapid and uneventful.

Conclusion: Dexmedetomidine and a small dose of propofol were used successfully to sedate a critically ill infant for MRI. More studies are required to determine the role of this unique drug in the pediatric population.

	Introduction

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SEDATING children for magnetic resonance imaging (MRI) poses many challenges due to the effects of the magnetic field. MRI sedation for small critically ill infants may require general anesthesia and controlled ventilation.¹ Dexmedetomidine, an alpha-₂ adrenergic agonist, has been used to provide sedation and analgesia postoperatively in surgical patients with minimal effect on respiration.² This case report describes a small infant with complex congenital heart disease (CHD) who received iv dexmedetomidine and propofol for MRI sedation while breathing spontaneously.

	Case report

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A nine-month-old, 5.1-kg infant was scheduled for MRI of the thorax under anesthesia. Medical history revealed a double outlet right ventricle and mitral atresia with single ventricle physiology. Initial surgical correction as a neonate consisted of placement of a Blalock-Taussig shunt. At age six months, the Blalock-Taussig shunt was revised and a bi-directional Glenn shunt was placed. The infant had a history of persistent bilateral chylous pleural effusions, which had been drained by computed tomography-assisted thoracentesis and chest tube placement. Small bilateral pleural effusions were present on chest radiograph. Recent cardiac catheterization demonstrated increased pulmonary artery pressure and possible pulmonary venous stenosis. MRI of the thorax was requested to further evaluate patency of the pulmonary venous system, a necessary condition for future consideration as a heart transplant recipient.

Physical examination in the MRI suite revealed an alert infant, with a functioning peripheral iv line, receiving 0.5 L·min^–1 supplemental oxygen via nasal cannula. Vital signs were: respiratory rate 25 breaths·min^–1, blood pressure 75/38 mmHg measured by cuff on the left thigh, heart rate 125 beats·min^–1, oxygen saturation 82%. After pretreatment with atropine 0.1 mg iv, a dexmedetomidine loading dose of 1 µg·kg^–1 iv was administered over ten minutes. At this point, 5 mg of iv propofol were administered to produce somnolence as the infant occasionally cried. A dexmedetomidine infusion of 0.5 µg·kg^–1·hr^–1 was started, and the infant was positioned in the MRI scanner. Oxygen at 4 L·min^–1 was administered by pediatric face mask with an end-tidal CO₂ sampling port affixed inside the mask. Soft foam ear muffs with adhesive backing were applied to abate noise from the MRI machine. Anesthetic conditions were excellent, with minimal change in vital signs during the entire 30 min duration of the scan. End-tidal CO₂ was initially 54 mmHg and stayed in the mid 50 range throughout the procedure. Once during the scan, the supplemental oxygen supply became accidentally disconnected from its source. Oxygen saturation briefly fell to 84%, similar to preoperative values, then rose again to 94% when oxygen was reconnected. Once the scan was completed, the infant was awake and responsive to light tactile stimulation within five minutes after the dexemedetomidine infusion was discontinued. Recovery was uneventful.

	Discussion

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Dexmedetomidine is an alpha-₂ adrenergic agonist with sedative, analgesic, and anxiolytic properties similar to clonidine, another alpha-₂ agonist.^3,4 Dexmedetomidine has seven times the alpha-₂ receptor specificity of clonidine; and is only available as a readily titratable iv drug with rapid onset. Its pharmacology and mechanism of action have been reviewed elsewhere.⁵ Briefly, alpha-₂ receptors modulate the activity of the autonomic nervous and cardiovascular systems. Activation of the alpha-₂ receptor in peripheral blood vessels causes vasoconstriction and, in the autonomic ganglia, stimulation of the receptor inhibits the release of catecholamines.^5,6 Activation of alpha-₂ receptors in the central nervous system, particularly in the locus ceruleus, may cause a significant reduction in central sympathetic flow and result in sedation and increased vagal activity.^7–9 Sedation with dexemedetomidine resembles light sleep. In contrast to other hypnotics, such as propofol, sedation with alpha-₂ agonists causes minimal respiratory depression and has little effect on the ventilatory response to an inhaled carbon dioxide challenge.^8,9

Dexmedetomidine is currently approved only for short-term (24 hr) sedation in intubated and mechanically ventilated adults in the intensive care unit. Experience with the use of dexmedetomidine in pediatric patients has been limited. In one study, sedation with a continuous infusion of dexemedetomidine at 0.25 µg·kg^–1·hr^–1 was comparable to midazolam 0.22 mg·kg^–1·hr^–1.6 At higher infusion rates (0.5 µg·kg^–1·hr^–1), sedation with dexemedetomidine was reported to be superior to midazolam, as measured by morphine requirements during the case.⁶ Of interest, these authors indicated that dexemedetomidine was less effective as a sedative in infants less than 12 months of age.⁶ This may be the reason why we needed to administer a small dose of propofol to produce somnolence in our infant. In a separate report, the same authors described a case of severe bradycardia (54 beats·min^–1) in a five-week-old infant (3.6 kg), who was also receiving digoxin, after 13 hr of constant rate infusion of dexemedetomidine, 0.5 µg·kg^–1·hr^–1.10 The authors speculated that a potential interaction between digoxin and dexemedetomidine may cause bradycardia. Nonetheless, because of the potential for increased cardiac activity with dexemedetomidine, we opted to pretreat the infant with atropine. It is important to note that the doses of dexemedetomidine required for sedation in pediatric patients are considerably lower than for adult patients, where the loading dose is typically 1 µg·kg^–1 followed by an infusion of 0.2 to 0.7 µg·kg^–1·hr^–1.9

No previous reports describe the use of dexemedetomidine as a sedative in infants with CHD who are not intubated and mechanically ventilated. MRI scans are not particularly stimulating procedures but do require the patient to remain perfectly still in order to obtain a good quality study. At our institution, the usual technique for sedating pediatric patients requiring anesthesia for an MRI would have been a propofol infusion with controlled ventilation. By using dexmedetomidine, we were able to maintain spontaneous ventilation during sedation which greatly simplified the anesthetic technique because of the magnetic fields related to MRI. No respiratory depression was detected, consistent with what has been observed with the use of dexmedetomidine in adults.⁷ It is nevertheless possible that we under-appreciated the potential for respiratory depression for two reasons. First, we measured ETCO₂ by a catheter placed in the mask. Measuring carbon dioxide using this technology may be affected by the flow rate of oxygen, turbulence under the mask, and leaks. Secondly, this infant had congenital cardiac lesions which may make it difficult to predict the true end-tidal to arterial carbon dioxide tension. However, other parameters of respiratory function were satisfactory. For instance, oxygen saturation was well maintained throughout, even with an inadvertent interruption in supplemental oxygen supply to the infant, and respiratory rate remained normal.

Anesthetic goals were accomplished with dexmedetomidine due to its unique pharmacology. Under the described conditions, dexmedetomidine infusion and a small initial dose of propofol provided excellent anesthetic conditions for an MRI procedure in a critically ill child. More studies are required to determine the utility of dexmedetomidine as a sedative for non-stimulating procedures in children.

	Footnotes

 
There is no conflict of interest to disclose.

Accepted for publication November 3, 2004. Revision accepted March 4, 2005.

	References

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1 Coté CJ. Anesthesia outside the operating room. In: Coté CJ, Todres ID, Ryan JF, Goudsouzian NG (Eds). A Practice of Anesthesia for Infants and Children, 3rd ed. Philadelphia: W.B. Saunders; 2001: 571–83.

2 Herr DL, Sum-Ping ST, England M. ICU sedation after coronary artery bypass graft surgery: dexmedetomidine-based versus propofol-based sedation regimens. J Cardiothorac Vasc Anesth 2003; 17: 576–84.[Medline]

3 Kamibayashi T, Maze M. Clinical uses of alpha₂-adrenergic agonists. Anesthesiology 2000; 93: 1345–9.[Medline]

4 Khan ZP, Ferguson CN, Jones RM. Alpha-2 and imidazoline receptor agonists. Their pharmacology and therapeutic role. Anaesthesia 1999; 54: 146–65.[Medline]

5 Scheinin H, Karhuvaara S, Olkkola KT, et al. Pharmacodynamics and pharmacokinetics of intramuscular dexmedetomidine. Clin Pharmacol Ther 1992; 52: 537–46.[Medline]

6 Tobias JD, Berkenbosch JW. Initial experience with dexmedetomidine in paediatric-aged patients. Paediatr Anaesth 2002; 12: 171–5.[Medline]

7 Venn RM, Hell J, Grounds RM. Respiratory effects of dexmedetomidine in the surgical patient requiring intensive care. Crit Care 2000; 4: 302–8.[Medline]

8 Nelson LE, Lu J, Guo T, Saper CB, Franks NP, Maze M. The alpha₂-adrenoceptor agonist dexmedetomidine converges on an endogenous sleep-promoting pathway to exert its sedative effects. Anesthesiology 2003; 98: 428–36.[Medline]

9 Tobias JD, Berkenbosch JW. Sedation during mechanical ventilation in infants and children: dexmedetomidine versus midazolam. South Med J 2004; 97: 451–5.[Medline]

10 Berkenbosch JW, Tobias JD. Development of bradycardia during sedation with dexmedetomidine in an infant concurrently receiving digoxin. Pediatr Crit Care Med 2003; 4: 203–5.[Medline]

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